ABSTRACT
Anatomical and physiological characteristics of fish are useful for studying control of exercise metabolism. In burst exercise, a high proportion of the body mass is recruited and its impact on whole body metabolism is profound. Recovery from burst exercise in fish requires much longer periods than mammals. Lactate metabolism occurs primarily within the white muscle and it is mostly converted to glycogen with little oxidation. Glycogen synthesis requires mitochondrial ATP, probably derived from oxidation of fatty acids. Fish white muscle is generally considered a mitochondria-poor tissue, and the rate of lactate removal across species (spanning 2 orders of magnitude) correlates with mitochondrial capacity of the white muscle. It is unlikely, however, that mitochondrial capacity limits the rate of recovery as there is manyfold excess aerobic capacity for the identifiable energy demands of recovery metabolism. Enzyme and metabolite measurements suggest that pyruvate kinase (PK) reversal is the likely pathway for glycogen resynthesis and argue that recovery may be limited by the capacity for PK reversal under physiologically achievable conditions. Although a high ATP/ADP ratio would suppress white muscle mitochondrial respiration throughout recovery, it should favor PK reversal. Direct evidence for reversal of PK is, at present, lacking.
